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GDF15 Restrains Myocardial Ischemia-reperfusion Injury Through Inhibiting GPX4 Mediated Ferroptosis

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Specialty Geriatrics
Date 2024 Jan 11
PMID 38206295
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Abstract

Background: Growth and differentiation factor 15 (GDF15) has been proved to regulate the process of Myocardial ischemia-reperfusion injury (MIRI), which is a serious complication of reperfusion therapy. The present study aimed to explore if GDF15 could regulate the MIRI-induced ferroptosis.

Method: MIRI animal model was established by ligating the left anterior descending coronary artery. Oxygen-glucose deprivation/reoxygenation (OGD/R) cell model was established to imitate MIRI . The indicators of ferroptosis including mitochondrial damage, GPX4, FACL4, XCT4, and oxidative stress markers were evaluated.

Results: Overexpression of GDF15 greatly inhibited MIRI, improved cardiac function, alleviated MIRI-induced ferroptosis. pc-DNA-GDF15 significantly inhibited the oxidative stress condition and inflammation response. The OGD/R-induced ferroptosis was also inhibited by pc-DNA-GDF15.

Conclusion: We proved that the MIRI-induced ferroptosis could by inhibited by pc-DNA-GDF15 through evaluating mitochondrial damage, MDA, GSH, and GSSG. Our research provides a new insight for the prevention and treatment of MIRI, and a new understanding for the mechanism of MIRI-induced ferroptosis.

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References
1.
Yang L, Jian Y, Zhang Z, Qi B, Li Y, Long P . Network-pharmacology-based research on protective effects and underlying mechanism of Shuxin decoction against myocardial ischemia/reperfusion injury with diabetes. World J Diabetes. 2023; 14(7):1057-1076. PMC: 10401449. DOI: 10.4239/wjd.v14.i7.1057. View

2.
Liu L, Pang J, Qin D, Li R, Zou D, Chi K . Deubiquitinase OTUD5 as a Novel Protector against 4-HNE-Triggered Ferroptosis in Myocardial Ischemia/Reperfusion Injury. Adv Sci (Weinh). 2023; 10(28):e2301852. PMC: 10558642. DOI: 10.1002/advs.202301852. View

3.
Zhang M, Pan K, Liu Q, Zhou X, Jiang T, Li Y . Growth differentiation factor 15 may protect the myocardium from no‑reflow by inhibiting the inflammatory‑like response that predominantly involves neutrophil infiltration. Mol Med Rep. 2015; 13(1):623-32. PMC: 4686086. DOI: 10.3892/mmr.2015.4573. View

4.
Pang P, Si W, Wu H, Ju J, Liu K, Wang C . YTHDF2 Promotes Cardiac Ferroptosis Degradation of SLC7A11 in Cardiac Ischemia-Reperfusion Injury. Antioxid Redox Signal. 2023; 40(16-18):889-905. DOI: 10.1089/ars.2023.0291. View

5.
Zhuang L, Zong X, Yang Q, Fan Q, Tao R . Interleukin-34-NF-κB signaling aggravates myocardial ischemic/reperfusion injury by facilitating macrophage recruitment and polarization. EBioMedicine. 2023; 95:104744. PMC: 10433018. DOI: 10.1016/j.ebiom.2023.104744. View